NO/cGMP signalling pathway represents one of the possible cross-talk mechanisms between myocytes and endothelial cells in macro- and microvessels. Recent data suggest that NO plays a key role in control of Ca2+ release from ryanodine- and IP3- sensitive Ca2+ stores. The functional link between Ca2+ release and IP3R phosphorylation has been established. These data suggest that Ca2+ oscillations mediated by IP3 and/or RyR channels could be potential targets of NO/cGMP pathway. In our recent work we have established that in myocytes of arcade arterioles there are two independent Ca2+ stores: one is sensitive to caffeine/ryanodine and the other to agonist/2-APB. In the present work we used 2-and 3-dimensional live confocal imaging of ureteric microvascular networks in situ to investigate interaction between endothelium Ca2+ signalling and Ca2+ signalling in myocytes induced by [Arg8]-Vasopressin (AVP, 5nM) and caffeine (0.5-2mM) of all sections of arteriolar networks. Caffeine induced irregular Ca2+ oscillations exclusively in myocytes of arcade arterioles, which appeared as propagating Ca2+ waves with variable spatial spread, selectively blocked by ryanodine (50µM). AVP induced Ca2+ oscillations in all sections of arteriolar network, which appeared as fully propagating recurrent Ca2+ waves. Ryanodine had no effect on AVP-induced Ca2+ oscillations in myocytes of all sections of arteriolar network, selectively inhibited by 2-APB (50 µM). Activation of endothelial Ca2+ signalling by 1µM CCh produced complete termination of the AVP-induced Ca2+ oscillations in myocytes of all sections of arteriolar network but had no effects on Ca2+ sparks and caffeine-induced Ca2+ oscillations in myocytes of arcade arterioles. L-NAME but not indomethacin prevented the inhibitory effect of endothelial Ca2+ signalling on AVP-induced Ca2+ oscillations in myocytes, suggesting that NO was involved. NO donor SNAP (20 µM) or SNP (20µM) produced quick and reversible inhibition of AVP-induced Ca2+ oscillations in myocytes of all sections of arteriolar network but had no effect on Ca2+ sparks and caffeine-induced Ca2+ oscillations in myocytes of arcade arterioles. The data obtained suggest that L-Arginine/NO pathway controls agonist induced Ca2+ oscillations in myocytes of arteriolar networks by selective inhibition of Ca2+ release via IP3R channels.